Can Autoimmune Conditions be Reversed? Researchers Make a Surprising Discovery

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It’s about time that everyone who suffers from an autoimmune condition got some good news.

The good news comes from researchers associated with Brigham and Women’s Hospital at Harvard Medical School. They recently completed a study focused on the immune system and autoimmune response.  In it, they identified a molecule that can “tune immune response and restore tissue integrity by activating stem cells.”i

Dr. Stefan G. Tullius, the lead study author, commented:

“This is a universal molecule that can potentially treat not only immune diseases, but other acute or chronic conditions…“ii

The results from this study promise more than pain relief. This molecule offers hope for the restoration of quality of living with the potential to reverse the conditions. The best news: anyone who wants to take advantage of this incredible molecule can do so today.

The Molecule that Rocks Autoimmune Conditions

One in five Americans suffers from auto-immune conditions according to the American Autoimmune Related Diseases Association.iii   This includes conditions like:

  • Chronic joint pain
  • Muscle weakness
  • Chronic gas, bloating, diarrhea and abdominal pain
  • Flare-ups of dry, scaly skin
  • High blood sugar

Anyone who suffers from these or any other autoimmune condition understands the pain, struggle and poor quality of life conditions like these can cause. While the exact causes of autoimmune conditions remain a mystery, researchers now have hope that they can treat these conditions.

It all starts with a molecule found in all living cells. That molecule is NAD+.

The Story Behind NAD+ and Autoimmunity

NAD+ fuels energy production in the mitochondria. In this way it is vital for every process in the human body, from metabolism to hormone regulation to immune system function. It also plays a role in other cellular processes including enzymatic reactions such as DNA repair. Without it, cells die.

This molecule occurs naturally in all human cells. The human body produces it through the conversion of the amino acid tryptophan or vitamin B3, although it turns out vitamin B3 has one significant drawback. As we age, our body produces less as the metabolism slows. The less that gets produced, the less there is to fuel energy production and immune system regulation as well.

Several years ago, researchers observed NAD+ appeared to have a much bigger role in immune response than previously thought. Some researchers noted it determined which immune cells participated in immune response and which do not.iv  Others reported its involvement in the process that determines the purpose of T-cells, immune cells that identify pathogens.v  Yet others saw that it turned inflammatory immune cells off and on through activation of the SIRT6 gene.vi

Other studies have also shown that a lack of regulatory immune cells consistently appear in autoimmune diseases.vii  This led researchers at Harvard Medical School to test what role NAD+ would have in autoimmune response. And it turns out NAD+ plays a much bigger role in the way immune cells work. Some of the team’s new discoveries even surprised them.

A Breakthrough in Autoimmune Response Research

For their experiment, the Harvard team tested NAD+ against an autoimmune condition in mice that causes nerve pain, muscle weakness and sore achy joints. The researchers induced nerve cell damage via immune response. Then they gave one group an injection of NAD+; the other group received a placebo.

The mice that received the NAD+ injection experienced a shift in their autoimmune response. The cells that attacked their nerves went from being destructive autoimmune cells to becoming protective immune cells. The NAD+ re-established balance in their immune systems.

Better yet, the physical damage done by the autoimmune attack reversed.viii  The damaged nerves of the mice experienced repair and healing. The researchers were also shocked when they observed certain immune system proteins known to play a role in inflammation act to limit inflammation with the application of NAD+.ix

These results prompted additional research to confirm these findings and look deeper into the changes:

  • A Chinese team duplicated the Harvard team’s experiment with specific attention to the role of the NAD+ reliant SIRT1 protein known for its role in preventing inflammation. As in the Harvard Medical School study, the immune response of the mice changed and their nerves repaired.
  • Researchers at the University of Maryland reported that the activation of the SIRT1 protein eased or even reversed the recurrence of joint and muscle pain and other chronic conditions that afflict nerve and brain cells.xi
  • In a more recent review of studies, researchers again from the University of Maryland found further evidence for the neuroprotective properties for SIRT1 and thereby NAD+.xii

The results of all of these studies suggest it may be possible to deactivate autoimmune response. The studies also show delivering NAD+ to cells affected by the autoimmune response can reverse damage. All of this offers incredible hope for and end to the pain, discomfort and health problems caused by autoimmune conditions.

Despite all the promise, one significant challenge remains.

The Challenge of NAD+ Supplementation

NAD+ supplements pose a challenge. As noted earlier, the human body can make its own NAD+ from tryptophan or vitamin B3. While these may work well for young, healthy individuals, they do not work as well for those who suffer from autoimmune conditions or for anyone who needs to substantially boost their NAD+ levels.

The best supplement to boost NAD+ levels looks to be a newly identified NAD+ building block: Nicotinamide mononucleotide or “NMN”.

Introducing ProHealth’s NMN Pro™

Nicotinamide mononucleotide (NMN) is a derivative of the B-vitamin niacin that dramatically improves health and longevity by serving as a precursor to NAD+.

When we boost NMN levels in the body, we can enhance the biosynthesis of NAD+ and alleviate symptoms associated with depletion of this crucial nutrient.

Lozenges Significantly Enhance NMN Bioavailability

NMN Pro™ features an innovative lozenge delivery system which increases the product’s bioavailability versus other delivery systems such as capsules or tablets.

  • Lozenges allow the supplement to be absorbed into the blood vessels underneath the tongue.
  • The NMN avoids digestion in the gastrointestinal tract and can be more rapidly delivered to the bloodstream.

Other Conditions Improved by NAD+

Long before researchers uncovered the connection between NAD+ and the immune system, it was known for its anti-aging effects. This effect came from its importance in energy production in the mitochondria, the energy centers in cells. Reduction of mitochondria directly relates to the physical symptoms we associate with aging, including inflammation, fatigue and brain fog.

NAD+ plays an indispensible role in the mitochondria. It carries an electron during the creation of ATP, the energy molecule. That may seem like a small role, but without it, ATP does not get produced.

Without ATP, mitochondria cannot produce energy. As a result, fewer mitochondria survive. Fewer mitochondria mean less energy and it reduces the ability of cells to do their job. While some cells only have one mitochondria, many cells have a lot more, up to 2,500 in those that require large amounts of energy like muscle and brain cells.

To produce energy, every one of these mitochondria requires a constant source of NAD+. If NAD+ levels fall, so too will the number of mitochondria. This reduces the body’s ability to convert tryptophan and produce NAD+.

This then creates a cycle of mitochondria decline. It’s no surprise then NAD+ levels fall as we age. It may be even less surprising that studies have shown symptoms of aging relate directly to low NAD+ levels.  Other conditions shown to relate to lower levels of NAD+ include higher blood sugar, weight gain, cardiovascular inflammation, loss of muscle strength and slower thinking and recall.

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* Copywriter Peter Rufa writes for a wide range of clients but specializes in health. He has written for doctors, supplement providers, healthcare, medical, and fitness organizations and businesses throughout the United States.

 

References:

[i] https://www.eurekalert.org/pub_releases/2014-10/bawh-anp100114.php

[ii] Ibid.

[iii] https://www.aarda.org/autoimmune-information/questions-and-answers/

[iv] Adriouch S1, Hubert S, Pechberty S, Koch-Nolte F, Haag F, Seman M. NAD+ released during inflammation participates in T cell homeostasis by inducing ART2-mediated death of naive T cells in vivo. J Immunol. 2007 Jul 1;179(1):186-94. https://www.ncbi.nlm.nih.gov/pubmed/17579037

[v] Hubert S1, Rissiek B, Klages K, Huehn J, Sparwasser T, Haag F, Koch-Nolte F, Boyer O, Seman M, Adriouch S. Extracellular NAD+ shapes the Foxp3+ regulatory T cell compartment through the ART2-P2X7 pathway. J Exp Med. 2010 Nov 22;207(12):2561-8. doi: 10.1084/jem.20091154. Epub 2010 Oct 25. https://www.ncbi.nlm.nih.gov/pubmed/20975043

[vi] Van Gool F1, Gallí M, Gueydan C, Kruys V, Prevot PP, Bedalov A, Mostoslavsky R, Alt FW, De Smedt T, Leo O. Intracellular NAD levels regulate tumor necrosis factor protein synthesis in a sirtuin-dependent manner. Nat Med. 2009 Feb;15(2):206-10. doi: 10.1038/nm.1906. Epub 2009 Jan 18. https://www.ncbi.nlm.nih.gov/pubmed/19151729

[vii] Buckner JH1. Mechanisms of impaired regulation by CD4(+)CD25(+)FOXP3(+) regulatory T cells in human autoimmune diseases. Nat Rev Immunol. 2010 Dec;10(12):849-59. doi: 10.1038/nri2889. https://www.ncbi.nlm.nih.gov/pubmed/21107346

[viii] Tullius SG, et al. NAD+ protects against EAE by regulating CD4+ T-cell differentiation. Nat Commun. 2014 Oct 7;5:5101. doi: 10.1038/ncomms6101. http://www.nature.com/articles/ncomms6101

[ix] Ibid.

[x] Wang J1, Zhao C1, Kong P1, Sun H2, Sun Z1, Bian G1, Sun Y1, Guo L3. Treatment with NAD(+) inhibited experimental autoimmune encephalomyelitis by activating AMPK/SIRT1 signaling pathway and modulating Th1/Th17 immune responses in mice. Int Immunopharmacol. 2016 Oct;39:287-94. doi: 10.1016/j.intimp.2016.07.036. Epub 2016 Aug 5. https://www.ncbi.nlm.nih.gov/pubmed/27500459\

[xi] Martin A1, Tegla CA, Cudrici CD, Kruszewski AM, Azimzadeh P, Boodhoo D, Mekala AP, Rus V, Rus H. Role of SIRT1 in autoimmune demyelination and neurodegeneration. Immunol Res. 2015 Mar;61(3):187-97. doi: 10.1007/s12026-014-8557-5. https://www.ncbi.nlm.nih.gov/pubmed/25281273

[xii] Nimmagadda VK1, et al. SIRT1 and NAD+ precursors: Therapeutic targets in multiple sclerosis a review. J Neuroimmunol. 2016 Jul 17. pii: S0165-5728(16)30158-8. doi: 10.1016/j.jneuroim.2016.07.007. [Epub ahead of print] https://www.ncbi.nlm.nih.gov/pubmed/27474445

[xiii] Trammell SA1, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun. 2016 Oct 10;7:12948. doi: 10.1038/ncomms12948. https://www.ncbi.nlm.nih.gov/pubmed/27721479

[xiv] Ryu D1, et al. NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation. Sci Transl Med. 2016 Oct 19;8(361):361ra139. https://www.ncbi.nlm.nih.gov/pubmed/27798264

[xv] Bogan KL1, Brenner C. Nicotinic acid, nicotinamide, and nicotinamide riboside: a molecular evaluation of NAD+ precursor vitamins in human nutrition. Annu Rev Nutr. 2008;28:115-30. doi: 10.1146/annurev.nutr.28.061807.155443. https://www.ncbi.nlm.nih.gov/pubmed/18429699

[xvi] Massudi H, Grant R, Braidy N, Guest J, Farnsworth B, Guillemin GJ. Age-Associated Changes In Oxidative Stress and NAD+ Metabolism In Human Tissue. Polymenis M, ed. PLoS ONE. 2012;7(7):e42357. doi:10.1371/journal.pone.0042357. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407129/

[xvii] Samuel A.J. Trammell1, Mark S. Schmidt1, Benjamin J. Weidemann1, Philip Redpath2, Frank Jaksch3, Ryan W. Dellinger3, Zhonggang Li4, E Dale Abel1,4, Marie E. Migaud1,2 & Charles Brenner1,4. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications. Published 10 Oct 2016, DOI: 10.1038/ncomms12948. https://www.ncbi.nlm.nih.gov/pubmed/27721479

[xviii] Ibid.

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